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Updated: Feb 3, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices
Published on: July 14, 2010
Distinct amyloid distribution patterns in amyloid positive subcortical vascular cognitive impairment
Hyemin Jang1,2, Jong-Yun Park3, Young Kyoung Jang1,2
1Departments of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Abstract:
Amyloid-β (Aβ) and cerebral small vessel disease (CSVD) commonly coexist. They can occur independently by chance, or may interact with each other. We aimed to determine whether the distribution of Aβ in subcortical vascular cognitive impairments (SVCI) patients can be classified by the underlying pathobiologies. A total of 45 11C-Pittsburgh compound B PET positive (PiB(+)) SVCI patients were included in this study. They were classified using a new cluster analysis method which adopted the Louvain method, which finds optimal decomposition of the participants based on similarity of relative Aβ deposition pattern. We measured atherosclerotic cerebral small vessel disease (CSVD) markers and cerebral amyloid angiopathy (CAA) markers. Forty-five PiB(+) SVCI patients were classified into two groups: 17 patients with the characteristic Alzheimer's disease like Aβ uptake with sparing of occipital region (OccSp) and 28 patients with occipital predominant Aβ uptake (OccP). Compared to OccSp group, OccP group had more postive association of atherosclerotic CSVD score (p for interaction = 0.044), but not CAA score with occipital/global ratio of PiB uptake. Our findings suggested that Aβ positive SVCI patients might consist of heterogeneous groups with combined CSVD and Aβ resulting from various pathobiologies. Furthermore, atherosclerotic CSVD might explain increased occipital Aβ uptakes.
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